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Na reabsorption
- active process
- 80% energy requirements for reabsorption
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Na reabsorption in proximal tubule
- crosses luminal membrane through co-transport with glucose, vitamins, amino acids
- crosses basolateral membrane through Na/K ATPase pumps
- glucose etc crosses through facilitated diffusion
- simple diffusion into capillary
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renal threshold
maximal plasma concentration of any organic nutrients before they begin to appear in the urine- spill over
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Na reabsorption in the ascending loop of Henle
- coupled to K and Cl in luminal membrane
- uses K/Na ATPase pump in the basolateral membrane
- simple diffusion into capillary
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Na reabsorption in the distal tubule
- coupled to Cl in the luminal membrane
- uses K/Na ATPase pump in basolateral membrane
- simple diffusion into capillary
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Na reabsorption in the Collecting duct
passive channels in the luminal membrane
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Mechanisms for passive water reabsorption
paracellular route
- coupled to sodium reabsorption, has to happen before water can move
- paracellular is in between epithelial cells, uses tight junctions
- microenvironments created from K/Na ATPase pumps , they have a higher osmolarity
- only in proximal tubule and descending loop of Henle
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mechanisms of passive water reabsorption
transcellular route
- coupled to NA reabsorption
- through epithelial cells, uses osmotic gradient btw luminal space and ISP
- requires aquaporins in luminal membrane that are created by ADH
- aquaporins are always available in the basolateral membrane
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Passive Chlorine reabsorption
- coupled to Na reabsorption, uses electrical gradient
- Na creates positive electrical gradient in the micro-environments
- Cl is drawn to the positive charge and is able to passively move across the luminal membrane
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substances that dont get reabsorbed
- waste products, except urea
- phenols, creatinine, nitrogen-containing wastes
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reabsorption in distal tubule and collecting duct
- hormonal regulation
- depends on secretion of ADH, aldosterone
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H+ secretion in the proximal tubule
- uses H+ and Na anti-porter, Na moves out of lumen into ISP
- H+ moves into lumen from capillary
- important part of acid-base balance
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H+ secretion in collecting duct/ loop of Henle
- use process of facilitated diffusion, ATPase pump in basolateral membrane and luminal membrane
- passive protein carrier
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K reabsorption in proximal tubule
- passive diffusion, similar to Cl and urea
- uses osmotic gradient
- unregulated
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K secretion in distal tubule and collecting duct
- active process, regulated
- simple diffusion across capillary, uses K/Na ATPase pump in basolateral membrane, both must be present for this pump to work
- uses K channels in luminal membrane
- promoted by aldosterone- enhances luminal transport mechanisms for Na, opens more channels to allow more K secretion
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descending loop permeability
- permeable to water
- impermeable to Na
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ascending loop permeability
- permeable to Na- actively pumped out
- impermeable to water
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osmolarity of urine at distal tubule
- 100 mOsm no matter our hydration status
- concentration happens in collecting duct
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stimulator for ADH secretion
- plasma osmolarity
- higher osmolarity= more ADH secretion
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Mechanism of Action of ADH
- enters blood stream, diffuses into ISP,
- binds to receptors on the basolateral membrane
- uses 2nd messenger to stimulate exocytosis of vesicles containing aquaporins
- aquaporins are inserted into luminal membrane so water can move into tubule- gradient must be present
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sensors for Na levels
baroreceptors, through sensation of arterial blood pressure via sensation of plasma blood volume
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Aortic arch and Carotid sinus baroreceptors
short term sensors, signal the onset of changes but adapt to sustained changes in BP
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Renal baroreceptors
- sense long term changes in BP
- located in granular cells in afferent arteriole
- sense BP and general perfusion in arteriole
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Renal baroreceptors MOA
- sense decrease in BP, which is decrease in plasma volume
- they release renin which is the rate limiting step in the production of angiotensin I, released from the granular cells
- angio I then is converted to Angio II in the lungs and is able to affect BP
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effects of Angiotensin II
- -acts on adrenal cortex to stimulate aldosterone release: regulates Na reabsorption at distal tubule and collecting duct
- -potent vasoconstrictor for both renal and systemic arteries, slows down overall GFR
- - reduces GFR by enhancing autoregulation, threshold decreases
- - enhances Na reabsorption by stimulating Na/H exchangers in proximal tubule
- - stimulates thirst and release of ADH to increase water absorption
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actions of Aortic and carotid baroreceptors
- raise sympathetic stimulation to kidneys in 2 main places
- -stimulate renal nerve to cause vasoconstriction of afferent arteriole, drop in GFR before angiotensin II takes over
- juxtaglomerular apparatus- triggers release of renin from granular cells before renal baroreceptors kick in
- SNS stimulation directly stimulates hypothalamus to release ADH
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results from a drop in BP
- immediately sensed by aortic and carotid baroreceptors
- causes release of renin, ADH due to increased sympathetic stimulation
- after a while the renal baroreceptors kick in and exert their effects
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osmoreceptors
- sense changes in plasma osmolarity, not CSF osmolarity
- central osmoreceptors are most important- SFO and OVLT, circumventricular organs
- they affect the level of thirst and renal conservation of water
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results of increase in plasma osmolarity
- less water in blood than solutes
- SFO and OVLT will sense rise and fire action potentials that lead to an increase in ADH secretion
- creates increased water reabsorption at the distal tubule and collecting duct
- this can create change in water levels alone, without affecting Na levels
- increase in ADH is linear with increase in osmolarity
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factors that affect Plasma ADH and osmolarity
- rate of ADH breakdown: metabolized by liver, disease will cause decreased breakdown
- pain, fear, trauma: significant activation of sympathetic nervous system will increase ADH secretion
- alcohol consumption: decreases plasma ADH, dehydrating effect of alcohol
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3 pressures involved in GFR
- capillary BP: pushing pressure coming from glomerular capillaries, promotes ultrafiltration, driving force for filtration, changeable
- plasma colloid osmotic pressure: exerted by proteins that cant pass barrier, pulling pressure working against filtration
- BC hydrostatic pressure: what moves into tubule, opposes filtration, small but positive net filtration pressure
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autoregulation: results of rise in BP
- capillary BP will rise, GFR will increase, flow through distal tubule will increase and this is sensed by the macula densa cells in the distal tubule,
- they tell the granular cells in the afferent arteriole to release vasomediators to vasoconstrict vessels to bring the GFR back to normal
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control mechanism 2 for GFR
- extrinsic sympathetic control: goal is to alter GFR, to override autoregulation
- affects smooth muscle of the afferent and efferent arterioles, NE is released and binds to alpha adrenergic receptors to cause vasoconstriction and reduce capillary BP and decrease GFR
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purpose of capillary bulk flow
- to regulate distribution of ECF between plasma and interstitial space
- includes intravascular space and interstitial space
- completely passive process, distribution depends on sum of forces
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ultrafiltration
fluid moving from intravascular to interstitial space
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reapsorption
fluid moving from interstitial to the intravascular space
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hydrostatic pressure
- pushing pressure, pushes out from wherever it originates from
- pressure exerted by fluid, found in both compartments
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interstitial hydrostatic pressure
will promote reabsorption, significant but not changing pressure
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intravascular hydrostatic pressure
- same as capillary blood pressure
- similar pushing force, promotes ultrafiltration
- significant and can change, due to precapillary sphincters
- direction of bulk flow is determined by capillary blood pressure
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Oncotic pressure
- osmotic pressure exerted by proteins b/c they can cross capillary wall,
- pulling pressure, needs fluid to balance the amount of proteins
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plasma oncotic pressure
- from inside the intravascular space, from plasma proteins that are inside the capillary and they cant get out,
- albumin levels are the strongest predictor of this pressure
- promotes reabsorption, helps to maintain plasma volume
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interstitial oncotic pressure
promotes ultrafiltration, under most circumstances this is nearly 0, or approaching 0 because albumin is not designed to get out of vasculature to exert pressure
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tubular maxiumum
maximal rate of absorption in the proximal tubule
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